抄録
The authors investigated the distribution and range of ependymal cell defects and dynamics of these defects in a group of patients with non-communicating hydrocephalus and in the controls without central nervous system lesions. Ependymal defects in the control group were found at specific sites in the lateral ventricles, namely, roof and medial wall of the anterior horn, lateral wall of the posterior horn, and ventral wall of the inferior horn and these defects occupied a wider range in the hydrocephalic group. The thickness of the ventricular wall in the hydrocephalic group was greater than that in the controls, due to subependymal glial proliferation, and this increase was especially marked in the area of ependymal defects. From the findings at the junctional areas of the ventricular wall with and without the ependymal cells, it was suggested that proliferation of the subependymal glial fibers was a major factor in the spread of the defects. In cases with edema in the periventricular white matter of the hydrocephalic group, the distribution of edema did not match the area of ependymal cell defects and was more localized than the defects.
